Results 211 to 220 of about 89,051 (286)

Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids

open access: yesMolecular Oncology, EarlyView.
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici   +8 more
wiley   +1 more source

Informed decision-making in prioritising product variants. [PDF]

open access: yesPeerJ Comput Sci
Borrego D   +3 more
europepmc   +1 more source

Multi‐omic profiling of squamous cell lung cancer identifies metabolites and related genes associated with squamous cell carcinoma

open access: yesMolecular Oncology, EarlyView.
Using multi‐omic characterization, we aimed to identify key regulators specific to squamous cell lung carcinoma (SqCC). SqCC‐specific differentially expressed genes were integrated with metabolics data. High expression of the creatine transporter SLC6A8, along with elevated creatine levels, appeared to be a distinct metabolic feature of SqCC.
Johan Staaf   +10 more
wiley   +1 more source

DynBlock: dynamic data encryption with Toffoli gate for IoT. [PDF]

open access: yesSci Rep
Haq M   +6 more
europepmc   +1 more source

In vitro properties of patient serum predict clinical outcome after high dose rate brachytherapy of hepatocellular carcinoma

open access: yesMolecular Oncology, EarlyView.
Following high dose rate brachytherapy (HDR‐BT) for hepatocellular carcinoma (HCC), patients were classified as responders and nonresponders. Post‐therapy serum induced increased BrdU incorporation and Cyclin E expression of Huh7 and HepG2 cells in nonresponders, but decreased levels in responders.
Lukas Salvermoser   +14 more
wiley   +1 more source

A New Version of the Stream Cipher SNOW

open access: bronze, 2003
Patrik Ekdahl, Thomas Johansson
openalex   +1 more source

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

open access: yesMolecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu   +18 more
wiley   +1 more source

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